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In December 2019, a devastated novel coronavirus, Severe Acute Respiratory Syndrome coronavirus-2 (SARS-CoV-2), was identified as the causative agent of the acute atypical cluster of pneumonia cases in the city of Wuhan, China [1]. In February 2020, the World Health Organization (WHO) named the disease COVID-19. Currently, the SARS-CoV-2 pandemic is of a scale not seen since the 1918 influenza pandemic and has already infected more than 156 million people worldwide and resulted in 3.2 million deaths, and cancer is a major risk factor for death associated with COVID-19. Although the predominant clinical presentation is with respiratory disease, Human coronaviruses exhibit neuroinvasive potential, and the systemic disorders that are the hallmark of COVID-19, such as hypoxia, inflammation, and acquired thrombophilia, may impose a high risk of CNS complications [2]. However, it is not clear which of these complications are consequences of direct neurological injury of SARS-CoV-2 or events secondary to the systemic dysfunctional state. New information about the neurological entities arising in patients with COVID-19 is needed to delineate better the clinical implications of this disease. We report a case of a patient with Hypoxic Leukoencephalopathy after Cardiocirculatory Arrest in patient SARS-CoV-2 and Severe Interstitial Pneumonia.

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Long SARS-CoV-2 with Hypoxic Leukoencephalopathy, Cardiocirculatory Arrest and Severe Interstitial Pneumonia: The Role of Timely Nuclear Magnetic Resonance for the Early Diagnosis and Regression of this Dramatic Complication